Influence of acid-base changes on carbachol- and potassium-induced contractions of taenia coli of the rabbit.
The influence of acid-base changes (variations of extracellular pH within the range 6.2-8.2 and parallel changes in (HCO3-) and PCO2 at constant external pH) on contractions induced by carbachol and K+ was studied on preparations from taenia coli of the rabbit. Extracellular acidosis increased the concentration of carbachol necessary to evoke a given muscle tension and reduced the maximum response. During a carbachol-induced contraction acidosis reduced and alkalosis enhanced muscle tension. Changes in extracellular pH within the range 6.2-8.2 did not affect the initial, rapid phase of the contraction induced by 145 mmol/l of K+. However, with 40-80 mmol/l of K+ acidosis reduced the phasic response. The tonic contraction following the initial phasic response in 145 mmol/l K+ was enhanced by extracellular acidosis and decreased by alkalosis, whereas at a K+-concentration of 70 mmol/l the amplitude of the tonic contraction was greater at pH 7.4 than at pH 6.2. Propranolol 10(-6) mmol/l did not affect the influence of extracellular pH upon the K+-contracture. An increase of both PCO2 and (HCO-3) at constant extracellular pH did not alter the response of the muscle to carbachol. The tonic contraction during K+-stimulation was diminished by a parallel increase in PCO2 and (HCO-3) and at 47 mmol/l (HCO-3) it was almost abolished. A rise in PCO2 from 5 to 14 kPa without changes in (HCO-3), which caused extracellular pH to drop from 7.4 to 6.3, increased the tonic contraction in the same way as a fall in extracellular pH alone. These results seem to indicate that extracellular acidosis within the pathophysiological range (1) decreases the sensitivity of the polarized smooth muscle membrane to cholinergic stimulation, (2) reduces: the rate of release of stored Ca++, the transmembrane flow of Ca++ into the muscle cell, and the rate of Ca++ inactivation or extrusion during K+-contraction. The reduction of the tonic contracture with increasing PCO2 and (HCO-3) at constant extracellular pH is most likely attributable to the (HCO-3) ion.
D000136:Acid-Base Equilibrium; D000818:Animals; D001639:Bicarbonates / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D002217:Carbachol / Q000494:pharmacology; D002245:Carbon Dioxide / Q000494:pharmacology; D003106:Colon / Q000502:physiology*; D005769:Gastrointestinal Motility; D006863:Hydrogen-Ion Concentration; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000502:physiology; D011188:Potassium / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011817:Rabbits
D001639:Bicarbonates; D002245:Carbon Dioxide; D002217:Carbachol; D011433:Propranolol; D011188:Potassium; D002118:Calcium